Cytogenetic findings in 303 mexican patients with de novo acute myeloblastic leukemia

In this report we show the chromosomal changes seen in a group of 303 Mexican patients with de novo Acute myeloblastic Leukemia (AML). Two hundred forty-two patients were diagnosed and treated at two hospitals affiliated with the Instituto Mexicano del Seguro Social (IMSS). These are the Centro Medico Nacional Siglo XXI and Centro Medico La Raza Hospitals; the remaining 61 patients were diagnosed and treated at the Hospital General de Mexico (HGM). Clonal abnormalities were detected in 75.6 percent of the patients; this result agrees with what has been reported in other large series of AML studies. The incidence of changes per hospital was similar in patients from the IMSS hospitals (72-75 percent), while an increase was seen in patients from the HGM (85.2 percent). The cromosomal changes seen in this study in order of frequency were: t(15;17)[18.8 percent], t(9;22)[9.2 percent], miscellaneous chromosomal changes (mainly rearrangementa of chromosomes 1,2,3,12 y 17) [8.2 percent], abnormalities of 16q22 [7.3 percent], t(8;21)[6.3 percent], -7/del(7q)[5.6 percent], t(6;9)[5.3 percent), and abnormalities of 11q23 [4.6 percent]. We reported an increase in the indicidence of certain types of chromosomal changes seen in cases of AML, in comparison with reports from other countries. These differences must not be disregarded. We support this finding when comparing distribution of changes in the population of patients seen in the IMSS hospitals with those from the HGM; the main difference lies in the socioeconomic level

Chronic myelocytic leukemia in accelerated phase with i(17) (q10) and loss p53 gene. Case report

Chronic myelogenous leukemia (CML) is a clonal disorder that presents with a stable period followed by an accelarated phase. The most frequent chromosomal abnormality described is t(9;22). Alterations of chromosome 17, where p53 is located, have been described during transformation. We studied a 23-year-old male who presented with chronic myelogenous leukemia. The karyotype demonstrated 46,XY,t(9;22) (q34;qll) in 12 percent of mitoses and hyperdiploidy in 43 percent. Forty six months later the patient suffered a blast crisis characterized by absolute basophilia; the cytogenetic study demonstrated 48,XY,+8,t(9;22(q34;qll), +der(22)t(9;22)(q34;qll),+i(17)(q10) in 18 percent of the mitoses, 46,XY,t(9;22) (q34;qll) in 34 percent and hyperdiploidy in 23 percent. Since there was i(17)(q10) during this stage, a retrospective DNA study of the biopsy material before and after the transformacition was performed. In the chronic phase, p53 was present in normal amounts, during transformation there was loss of genetic material from the p53 region. The protein product of suppressor gene p53 normally works holding the proliferation of cells. When there is the formation of an isochromosome, genetic material is lost; thus, in this patient, p53 was delted upon the observation of i(17). Lastly, this case shows how DNA can be extracted from slides; this technique is novel and can be used for retrospective studies when parafin block or fresh tissue are not available